Replies to post #238083 on Anavex Life Sciences Corp (AVXL)

[nidan7500]

Xena, Is this what I think it is? Much is beyond me but the repeats are playing back in one comprehensive piece what we have seen bits of here for years.

Thanks for spectacular work.

“A new study from Massachusetts General Hospital (MGH) investigators provides additional evidence that amyloid-beta protein -- which is deposited in the form of beta-amyloid plaques in the brains of patients with Alzheimer's disease -- is a normal part of the innate immune system, the body's first-line defense against infection. Their study published in Science Translational Medicine finds that expression of human amyloid-beta (A-beta or Aß) was protective against potentially lethal infections in mice, in roundworms and in cultured human brain cells. The findings may lead to potential new therapeutic strategies and suggest limitations to therapies designed to eliminate amyloid plaques from patient's brains.” https://www.sciencedaily.com/releases/2016/05/160525161351.htm

Why is this important? I believe that the formation of Aß is something “regulated” by the cells and by various organisms from humans to roundworms. Given how conserved the function of the enzymes are for cutting apart APP into small peptides, it seems logical that not only does APP have many roles in the cell, but that Aß must also. The recent study that Aß helps fight certain disease leads credence to this.

Therefore it is possible that the accumulation of Aß may be a consequence of cellular misregulation or due to inflammation processes. If a cell is “inflamed”, it may be undergoing an immune reaction where the cell is reacting to what it believes is an infection or attack. A younger healthier person has more robust regulation of cellular mechanisms due to producing higher concentrations of regulatory, hormones, having better circulation, having better metabolic regulation and better overall health. Therefore, the brains of younger people recover from such inflammation processes while the brains of older people sometime don't. Instead, the inflammation triggers other problems causing the cascade of issues ultimately leading to full blown Alzheimer’s disease.

Drugs that target Aß have not been effective because the misregulation of cellular mechanisms is not corrected by drugs that target Aß. And in fact, targeting Aß may make the misregulation issues worse. Just as too much Aß is a problem, too little may also be a problem.

Anavex2-73 does not target Aß directly. Rather, the impact is to signal the cell that it is under “stress” and should change cellular behavior in ways to reduce the stress and help the cell return to homeostasis.

The way it does this is mainly as a Sigma-1 Receptor (S1R) agonist and mixed muscarinic receptor agonist. The most widely known of those is the S1R which is what is called a receptor chaperone. For example, one of several functions is to modulate calcium signaling in the cell. Other changes in the receptor can signal the cell to die via programmed cell death (apoptosis) or signal it to try to recover and fight disease processes leading towards homeostasis.

See Anavex presentation slide diagram, “S1R = Sigma-1 Receptor”

https://www.sciencedaily.com/releases/2016/05/160525161351.htm

[attilathehunt]

The last two sentences says it all...

Alzheimer's after age 70 who takes a high dose of AVXL 2-73 would be able to live out their life until death with a much lower reduction in ability to think and remember. This would result in patients still remembering their life while being able to live on their own if they are otherwise healthy enough to do so.

[powerwalker]

Xena and amstock ... AWESOME!!!

Thank you for all that each of you do, especially the Anavex's warrior!!!